Abstract

Background

Sudden cardiac death resulting from acute myocardial infarction (AMI) constitutes
a significant percentage of the caseload for forensic and clinical pathologists. When
sudden death occurs at an early stage (<6 h), pathologists experience difficulty in
the postmortem diagnosis of AMI. Because of the specific tissue distribution of S100A1
and its relationship with acute ischemic heart disease, this study aimed to evaluate
the performance of S100A1 in the postmortem diagnosis of AMI.

Methods

We constructed a rat model of AMI through permanent ligation of the left anterior
descending coronary artery (LAD) to investigate the depletion of S100A1 from ischemic
cardiomyocytes by immunohistochemistry and measuring S100A1 plasma concentrations
by enzyme-linked immunosorbent assay at varying post-infarction intervals. In addition,
immunohistochemical staining of S100A1 for definite infarction, suspected early infarction,
and in normal human hearts, was also performed to test its practical feasibility for
postmortem diagnosis of AMI at an early stage.

Results

As early as 15 min after ligation of the LAD, depletion of S100A1 was observed in
ischemic cardiomyocytes, and S100A1 plasma concentration was also significantly higher
than that of the sham-operated group (P < 0.001). With continuation of the occlusion time, the depleted areas of S100A1 further
expanded and S100A1 plasma concentrations further increased. For autopsy material,
all human cases of definite myocardial infarction and suspected early infarction showed
well-defined areas without S100A1 staining. None of the normal human cases showed
diffuse depletion of S100A1.

Conclusion

Our results suggest that immunohistochemical detection of S100A1 is useful for the
postmortem diagnosis of AMI at an early stage.